Respiratory Flashcards

1
Q

Asbestos diseases

A

Pleural plaques (lower lungs and diaphragm, collagen and calcium, usually asymptomatic).
Asbestosis (progressive diffuse pulmonary fibrosis and the presence of asbestos bodies).
Bronchogenic carcinoma (most common malignancy of asbestos exposure).
Malignant mesothelioma.

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2
Q

What is primarily damaged in chronic lung transplant rejection?

A

The small bronchioles (bronchiolitis obliterans). Inflammation and fibrosis of the bronchiolar walls leads to narrowing and obstruction of the affected bronchioli. This leads to an obstructive pattern on spirometry.

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3
Q

Increased expiratory flow rates in pulmonary fibrosis are explained by an increase in what parameter?

A

Increased radial traction on airway walls (the fibrosis pulls the the airways)

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4
Q

What will a nasal transepithelial potential difference measurements show in a patient with cystic fibrosis?

A

A transepithelial potential difference that is more negative than normal. This is due to increased sodium absorption ( the test is performed by applying sodium chloride to the nasal mucosal surface and the electrical potential is measured compared to the interstium). The impaired CFTR protein causes a decrease in chloride secretion, so more sodium (and water) is absorbed via ENaC channels in the nasal mucosa. The chloride administered in the test will remain in the lumen of the nose, causing a negative potential.

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5
Q

What is zone 1 of the lung?

A

Does not occur in the lung under normal physiologic conditions, but would be found at the apex. Alveolar pressure > arterial pressure > venous pressure. Because the arterial pressure is lower than alveolar pressure, the pulmonary capillaries are collapsed and there is no blood flow (i.e. zone 1 represents alveolar dead space). This can happen when pulmonary arterial pressure is low (e.g. hemorrhage) or there is high alveolar pressure (e.g. positive-pressure ventilation).

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6
Q

What is zone 2 of the lung?

A

Found in higher areas of the lung like the apex. Arterial pressure > alveolar pressure > venous pressure. Because alveolar pressure is greater than venous pressure, the pulmonary capillaries are initially obstructed near the venous end of the capillary bed. However, as arterial pressure rises during systole, capillary pressure becomes high enough to overcome alveolar pressure. Blood flow through zone 2 moves in a pulsatile fashion.

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7
Q

What is zone 3 of the lung?

A

In lower areas of the lung. Arteriolar pressure> venous pressure > alveolar pressure. This means that blood flows continuously through capillaries. When a person is supine, the entire lung is composed of zone 3 blood blow.

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8
Q

What is responsible for the green color in pus or sputum in bacterial infections (e.g. pneumonia)

A

Neutrophil myeloperoxidase

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9
Q

What is primarily damaged due to acute lung transplant rejection?

A

Pulmonary and bronchial vessels.

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10
Q

What is the equation for surface tension?

A

P=2T/r. This is why smaller alveoli collapse when connected to larger ones if there is no surfactant.

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11
Q

What are common respiratory causes of pulsus paradoxus in the absence of significant pericardial disease (pericardial effusion or constrictive pericarditis)?

A

Asthma and COPD exacerbations. These patients have an exaggerated drop in intrathoracic pressure during inspiration.

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12
Q

What is Winter’s formula?

A

1.5[HCO3⁻] +8 ±2

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13
Q

What is the cause of primary spontaneous pneumothoraxes in young tall men?

A

The formation and subsequent rupture of apical subpleural blebs. Smoking and tall height (more negative intrapleural pressure in the lung apices) predisposes these individuals. Rupture of the blebs can cause a break in the visceral pleura which causes air to get trapped between the parietal and visceral pleura.

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14
Q

What is the pH, PaO2, PaCO2 and serum bicarb in a patient with pulmonary embolism?

A

Pattern of respiratory alkalosis: Increased pH, decreased PaO2, decreased PaCO2, bicarb is normal in the acute setting (will decrease after 48 hrs). This is due to a V/Q mismatch in which there is decreased perfusion. The hypoxemia stimulates the respiratory drive leading to hyperventilation. This does not significantly improve oxygenation, but will cause more CO2 to be excreted.

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15
Q

How is the pulmonary capillary wedge pressure affected in ARDS?

A

The pressure stays within normal limits usually. What does change is capillary permeability (leakier). This leads to decreased lung compliance (hyaline membrane formation), increased work of breathing, and worsened ventilation to perfusion mismatching.

An elevated PCWP is more suggestive of cardiogenic pulmonary edema (e.g. decompensated left ventricular failure).

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16
Q

What cytokine recruits eosinophil in chronic eosinophilic bronchitis?

A

IL-5 secreted by Th2 cells. Sputum samples may be described as containing cells with granules (eosinophils) and crystaloid bodies (Charcot-Leyden crystals that are composed of eosinophil membrane protein). These patients may have asthma attacks in the absence of triggers (extrinsic allergic asthma).

17
Q

What is the histology of mesothelioma?

A

Epitheliod cells held together by desmosomes, long slender microvilli, and abundant tonofilaments (keratin intermediate filaments).
Grossly, there will be nodular and smooth pleural thickening.

18
Q

What conditions is Cheyne-Stokes breathing seen in?

A

Congestive heart failure (especially during sleep due to cyclic hyperventilation due to hypercapnia) and neurologic disease (e.g. stroke, brain, tumors, traumatic brain injury).

19
Q

How does silicosis affect the pathogenesis of TB infections?

A

Impairs macrophage function due to ingestion of silica particles. This causes release of bacteria from damaged macrophages.

20
Q

What cell type is responsible for the elevated serum calcium in sarcoidosis?

A

Macrophages (activated macrophages have 1-alpha-hydroxylase which converts 25-hydroxyvitamin D to 1,25-hydroxyvitamin D)

21
Q

What is bosentan and what is it used for?

A

It is an endothelin-receptor antagonist that acts as a vasodilator (endothelin is a potent vasoconstrictor). It can be used to treat idiopathic or familial pulmonary arterial hypertension. Bosentan therapy decreases pulmonary arterial pressure and lessens the progression of vascular and right ventricular hypertrophy